Critical Care Medicine-Renal, Electrolyte and Acid Base Disorders>>>>>Acid Base Disorders
Question 8#

A 72-year-old woman with a past medical history of hypertension, hyperlipidemia, and congestive heart failure (most recent echocardiogram 3 months ago showed an ejection fraction of 45%) is intubated in the ICU for septic shock in the setting of Escherichia coli bacteremia. She received 9 L total of IV fluids, and on examination, she is awake and cooperative, though she has anasarca. She is unable to be weaned off the ventilator due to high respiratory rate, and a chest x-ray obtained shows bilateral vascular congestion. She is given furosemide over the next few days and started on enteral feedings.

After 3 days, repeat laboratory data show the following: 

• Sodium 146 mEq/L (mmol/L)
• Potassium 3.2 mEq/L (mmol/L)
• Chloride 110 mEq/L (mmol/L)
• Bicarbonate 16 mEq/L (mmol/L)
• Glucose 143 mg/dL
• BUN 27 mg/dL
• Creatinine 1.2 mg/dL
• Albumin 4.1 g/L
• Calcium 9.8 mg/dL

ABG:

• pH 7.48
• pCO₂ 45 mm Hg

Which of the following is MOST likely the cause of her acid-base disturbances?

A. Bartter syndrome
B. Diuretic usage
C. Primary respiratory acidosis
D. Milk-Alkali syndrome
E. RTA type 2

Correct Answer is B

Comment:

Correct Answer: B

The patient has primary metabolic alkalosis which is most likely due to diuretic usage. Diuretics such as furosemide increase sodium and water delivery to the distal nephron, which subsequently increases the urinary hydrogen and potassium secretion, thereby leading to metabolic alkalosis and hypokalemia. Furthermore, the contraction of extracellular fluid (ECF) leads to renin and aldosterone secretion, which slows the sodium loss but in turn increases the secretion of potassium and hydrogen ions. This is also known as “contraction alkalosis” which is due to the loss of low bicarbonate–containing extracellular fluid.

Patients with Bartter syndrome will have similar findings, but with the recent usage of diuretics and lack of previous history, this is less likely the cause here. Treatment consists of replacement of potassium chloride. 

References:

1. Greenberg A. Diuretic complications. Am J Med Sci. 2000;319(1):10-24.
2. Sica DA, Carter B, Cushman W, Hamm L. Thiazide and loop diuretics. J Clin Hypertens. 2011;13(9):639-643.